Pathobiology of liver fibrosis: a translational success story
Reversibility of hepatic fibrosis and cirrhosis following antiviral therapy for hepatitis B or C has advanced the prospect of developing antifibrotic therapies for patients with chronic liver diseases, especially non-alcoholic steatohepatitis. Mechanisms of fibrosis have focused on hepatic stellate...
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| Published in | Gut Vol. 64; no. 5; pp. 830 - 841 |
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| Main Authors | , , |
| Format | Journal Article Book Review |
| Language | English |
| Published |
England
BMJ Publishing Group LTD
01.05.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Reversibility of hepatic fibrosis and cirrhosis following antiviral therapy for hepatitis B or C has advanced the prospect of developing antifibrotic therapies for patients with chronic liver diseases, especially non-alcoholic steatohepatitis. Mechanisms of fibrosis have focused on hepatic stellate cells, which become fibrogenic myofibroblasts during injury through ‘activation’, and are at the nexus of efforts to define novel drug targets. Recent studies have clarified pathways of stellate cell gene regulation and epigenetics, emerging pathways of fibrosis regression through the recruitment and amplification of fibrolytic macrophages, nuanced responses of discrete inflammatory cell subsets and the identification of the ‘ductular reaction’ as a marker of severe injury and repair. Based on our expanded knowledge of fibrosis pathogenesis, attention is now directed towards strategies for antifibrotic therapies and regulatory challenges for conducting clinical trials with these agents. New therapies are attempting to: 1) Control or cure the primary disease or reduce tissue injury; 2) Target receptor-ligand interactions and intracellular signaling; 3) Inhibit fibrogenesis; and 4) Promote resolution of fibrosis. Progress is urgently needed in validating non-invasive markers of fibrosis progression and regression that can supplant biopsy and shorten the duration of clinical trials. Both scientific and clinical challenges remain, however the past three decades of steady progress in understanding liver fibrosis have contributed to an emerging translational success story, with realistic hopes for antifibrotic therapies to treat patients with chronic liver disease in the near future. |
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| AbstractList | Reversibility of hepatic fibrosis and cirrhosis following antiviral therapy for hepatitis B or C has advanced the prospect of developing antifibrotic therapies for patients with chronic liver diseases, especially non-alcoholic steatohepatitis. Mechanisms of fibrosis have focused on hepatic stellate cells, which become fibrogenic myofibroblasts during injury through 'activation', and are at the nexus of efforts to define novel drug targets. Recent studies have clarified pathways of stellate cell gene regulation and epigenetics, emerging pathways of fibrosis regression through the recruitment and amplification of fibrolytic macrophages, nuanced responses of discrete inflammatory cell subsets and the identification of the 'ductular reaction' as a marker of severe injury and repair. Based on our expanded knowledge of fibrosis pathogenesis, attention is now directed towards strategies for antifibrotic therapies and regulatory challenges for conducting clinical trials with these agents. New therapies are attempting to: 1) Control or cure the primary disease or reduce tissue injury; 2) Target receptor-ligand interactions and intracellular signaling; 3) Inhibit fibrogenesis; and 4) Promote resolution of fibrosis. Progress is urgently needed in validating non-invasive markers of fibrosis progression and regression that can supplant biopsy and shorten the duration of clinical trials. Both scientific and clinical challenges remain, however the past three decades of steady progress in understanding liver fibrosis have contributed to an emerging translational success story, with realistic hopes for antifibrotic therapies to treat patients with chronic liver disease in the near future. |
| Author | Wallace, Michael C Friedman, Scott L Lee, Youngmin A |
| Author_xml | – sequence: 1 givenname: Youngmin A surname: Lee fullname: Lee, Youngmin A email: Scott.Friedman@mssm.edu – sequence: 2 givenname: Michael C surname: Wallace fullname: Wallace, Michael C email: Scott.Friedman@mssm.edu – sequence: 3 givenname: Scott L surname: Friedman fullname: Friedman, Scott L email: Scott.Friedman@mssm.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25681399$$D View this record in MEDLINE/PubMed |
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| CODEN | GUTTAK |
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| IngestDate | Tue Sep 17 21:06:48 EDT 2024 Tue Aug 27 04:32:54 EDT 2024 Fri Aug 16 22:49:21 EDT 2024 Thu Oct 10 17:22:23 EDT 2024 Fri Aug 23 00:55:16 EDT 2024 Sat Sep 28 08:48:52 EDT 2024 Tue Nov 26 19:35:38 EST 2024 |
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| Issue | 5 |
| Keywords | FATTY LIVER EXTRACELLULAR MATRIX HEPATIC STELLATE CELL CIRRHOSIS HEPATIC FIBROSIS |
| Language | English |
| License | Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Article-1 ObjectType-Feature-2 YL and MCW contributed equally. |
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| SubjectTerms | Chronic illnesses Clinical trials Clinical Trials as Topic - methods Drug Discovery - methods Family medical history Fibroblasts Gastrointestinal surgery Growth factors Hepatic Stellate Cells - physiology Hepatitis Hepatitis B virus Humans Liver cancer Liver cirrhosis Liver Cirrhosis - drug therapy Liver Cirrhosis - pathology Liver diseases Mortality Patient Selection Rodents Stem cells Translational Medical Research - methods |
| Title | Pathobiology of liver fibrosis: a translational success story |
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